Stumvoll M, Chintalapudi U, Perriello G, Welle S, Gutierrez O, Gerich J
University of Rochester School of Medicine, Department of Medicine, New York 14642, USA.
J Clin Invest. 1995 Nov;96(5):2528-33. doi: 10.1172/JCI118314.
Despite ample evidence that the kidney can both produce and use appreciable amounts of glucose, the human kidney is generally regarded as playing a minor role in glucose homeostasis. This view is based on measurements of arteriorenal vein glucose concentrations indicating little or no net release of glucose. However, inferences from net balance measurements do not take into consideration the simultaneous release and uptake of glucose by the kidney. Therefore, to assess the contribution of release and uptake of glucose by the human kidney to overall entry and removal of plasma glucose, we used a combination of balance and isotope techniques to measure renal glucose net balance, fractional extraction, uptake and release as well as overall plasma glucose appearance and disposal in 10 normal volunteers under basal postabsorptive conditions and during a 3-h epinephrine infusion. In the basal postabsorptive state, there was small but significant net output of glucose by the kidney (66 +/- 22 mumol.min-1, P = 0.016). However, since renal glucose fractional extraction averaged 2.9 +/- 0.3%, there was considerable renal glucose uptake (2.3 +/- 0.2 mumol.kg-1.min-1) which accounted for 20.2 +/- 1.7% of systemic glucose disposal (11.4 +/- 0.5 mumol.kg-1.min-1). Renal glucose release (3.2 +/- 0.2 mumol.kg-1.min-1) accounted for 27.8 +/- 2.1% of systemic glucose appearance (11.4 +/- 0.5 mumol.kg-1.min-1). Epinephrine infusion, which increased plasma epinephrine to levels observed during hypoglycemia (3722 +/- 453 pmol/liter) increased renal glucose release nearly twofold (5.2 +/- 0.5 vs 2.8 +/- 0.1 mol.kg-1.min-1, P = 0.01) so that at the end of the infusion, renal glucose release accounted for 40.3 +/- 5.5% of systemic glucose appearance and essentially all of the increase in systemic glucose appearance. These observations suggest an important role for the human kidney in glucose homeostasis.
尽管有充分证据表明肾脏既能产生又能利用相当数量的葡萄糖，但一般认为人类肾脏在葡萄糖稳态中所起的作用较小。这一观点基于对肾动脉静脉葡萄糖浓度的测量，结果显示几乎没有或根本没有葡萄糖的净释放。然而，基于净平衡测量的推断并未考虑到肾脏同时进行的葡萄糖释放和摄取。因此，为了评估人类肾脏葡萄糖释放和摄取对血浆葡萄糖整体进入和清除的贡献，我们采用平衡和同位素技术相结合的方法，在基础空腹状态下以及3小时肾上腺素输注期间，测量了10名正常志愿者的肾脏葡萄糖净平衡、分数提取、摄取和释放以及血浆葡萄糖的整体出现和处置情况。在基础空腹状态下，肾脏有少量但显著的葡萄糖净输出（66±22 μmol·min⁻¹，P = 0.016）。然而，由于肾脏葡萄糖分数提取平均为2.9±0.3%，肾脏有相当数量的葡萄糖摄取（2.3±0.2 μmol·kg⁻¹·min⁻¹），占全身葡萄糖处置量（11.4±0.5 μmol·kg⁻¹·min⁻¹）的20.2±1.7%。肾脏葡萄糖释放（3.2±0.2 μmol·kg⁻¹·min⁻¹）占全身葡萄糖出现量（11.4±0.5 μmol·kg⁻¹·min⁻¹）的27.8±2.1%。肾上腺素输注使血浆肾上腺素水平升高至低血糖时观察到的水平（3722±453 pmol/升），使肾脏葡萄糖释放增加近两倍（5.2±0.5对2.8±0.1 μmol·kg⁻¹·min⁻¹，P = 0.01），因此在输注结束时，肾脏葡萄糖释放占全身葡萄糖出现量的40.3±5.5%，并且基本上占全身葡萄糖出现量增加的全部。这些观察结果表明人类肾脏在葡萄糖稳态中起着重要作用。
